CD39 limits P2X7 receptor inflammatory signaling and attenuates sepsis-induced liver injury.

ABSTRACT:

Background & aims

The severity of sepsis can be linked to excessive inflammatory responses resulting in hepatic injury. P2X7 receptor activation by extracellular ATP (eATP) exacerbates inflammation by augmenting cytokine production; while CD39 (ENTPD1) scavenges eATP to generate adenosine, thereby limiting P2X7 activation and resulting in A_2A receptor stimulation. We aim to determine how the functional interaction of P2X7 receptor and CD39 control the macrophage response, and consequently impact on sepsis and liver injury.

Methods

Sepsis was induced by cecal ligation and puncture in C57BL/6 wild-type (WT) and CD39^-/- mice. Several in vitro assays were performed using peritoneal or bone marrow derived macrophages to determine CD39 ectonucleotidase activi

SUBMITTER: Savio LEB 

PROVIDER: S-EPMC5875702 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature